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Air pollution and cytokine responsiveness in asthmatic and non-asthmatic children
Epidemiological studies indicate that asthmatic children are more susceptible to traffic-related air pollution exposure than non-asthmatic children. Local and systemic inflammation in combination with oxidative stress have been suggested as a possible susceptibility factor. We investigated effect mo...
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| Published in: | Environmental research 2015-04, Vol.138, p.381-390 |
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| creator | Klümper, Claudia Krämer, Ursula Lehmann, Irina von Berg, Andrea Berdel, Dietrich Herberth, Gunda Beckmann, Christina Link, Elke Heinrich, Joachim Hoffmann, Barbara Schins, Roel P.F. |
| description | Epidemiological studies indicate that asthmatic children are more susceptible to traffic-related air pollution exposure than non-asthmatic children. Local and systemic inflammation in combination with oxidative stress have been suggested as a possible susceptibility factor.
We investigated effect modification by asthma status for the association between air pollution exposure and systemic effects using whole blood cytokine responsiveness as an inflammatory marker.
The study was nested within the two German birth cohort studies GINIplus and LISAplus and initially designed as a random sub-sample enriched with asthmatic children. Using data from 27 asthmatic and 59 non-asthmatic six-year-old children we measured the production of Interleukin-6 (IL)-6, IL-8, IL-10, monocyte chemotactic protein-1 (MCP-1), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in whole blood after ex-vivo stimulation with urban particulate matter (EHC-93). Air pollution exposure (nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter with an aerodynamic diameter |
| doi_str_mv | 10.1016/j.envres.2015.02.034 |
| format | article |
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We investigated effect modification by asthma status for the association between air pollution exposure and systemic effects using whole blood cytokine responsiveness as an inflammatory marker.
The study was nested within the two German birth cohort studies GINIplus and LISAplus and initially designed as a random sub-sample enriched with asthmatic children. Using data from 27 asthmatic and 59 non-asthmatic six-year-old children we measured the production of Interleukin-6 (IL)-6, IL-8, IL-10, monocyte chemotactic protein-1 (MCP-1), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in whole blood after ex-vivo stimulation with urban particulate matter (EHC-93). Air pollution exposure (nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter with an aerodynamic diameter <10μm (PM10), particulate matter with an aerodynamic diameter <2.5μm (PM2.5mass), coarse particulate matter (PMcoarse) and PM2.5absorbance (PM2.5abs)) was modelled for children´s home addresses applying land-use regression. To assess effect modification by asthma status linear regression models with multiplicative interaction terms were used.
In asthmatics exposure to NO2 was associated with higher production of pro-inflammatory cytokines: adjusted means ratio (MR) 2.22 (95% confidence interval 1.22–4.04) for IL-6 per 2.68µg/m³ NO2. The interaction term between asthma status and NO2 exposure was significant. Results for NOx, PM10, PM2.5mass and PM2.5abs were in the same direction. No association between air pollution and cytokine responsiveness was found in the group of non-asthmatic children and in the overall group.
Traffic-related air pollution exposure is associated with higher pro-inflammatory cytokine responsiveness in whole blood of asthmatic children.
•We investigated the association between TRAP and systemic inflammation in asthmatic and non-asthmatic children.•Whole blood cytokine responsiveness was used as inflammatory marker.•TRAP is associated with higher pro-inflammatory cytokine responsiveness in asthmatic children.•No association was found in non-asthmatics.</description><identifier>ISSN: 0013-9351</identifier><identifier>EISSN: 1096-0953</identifier><identifier>DOI: 10.1016/j.envres.2015.02.034</identifier><identifier>PMID: 25769127</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Air Pollutants - blood ; Air pollution ; Asthma ; Asthma - chemically induced ; Asthma - epidemiology ; Blood ; Child ; Children ; Cohort Studies ; Cytokines ; Cytokines - metabolism ; Environmental Exposure ; Environmental Monitoring ; Exposure ; Female ; Flow Cytometry ; Germany - epidemiology ; Humans ; Inflammatory markers ; Male ; Models, Theoretical ; Nitrogen dioxide ; Nitrogen Oxides - blood ; Particle Size ; Particulate Matter - blood ; Regression ; Vehicle Emissions - analysis ; Whole blood assay</subject><ispartof>Environmental research, 2015-04, Vol.138, p.381-390</ispartof><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-65a92771d11ea099334e927e3e201e126b7c73338fde2d1b4df7907deb51e4f23</citedby><cites>FETCH-LOGICAL-c428t-65a92771d11ea099334e927e3e201e126b7c73338fde2d1b4df7907deb51e4f23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25769127$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Klümper, Claudia</creatorcontrib><creatorcontrib>Krämer, Ursula</creatorcontrib><creatorcontrib>Lehmann, Irina</creatorcontrib><creatorcontrib>von Berg, Andrea</creatorcontrib><creatorcontrib>Berdel, Dietrich</creatorcontrib><creatorcontrib>Herberth, Gunda</creatorcontrib><creatorcontrib>Beckmann, Christina</creatorcontrib><creatorcontrib>Link, Elke</creatorcontrib><creatorcontrib>Heinrich, Joachim</creatorcontrib><creatorcontrib>Hoffmann, Barbara</creatorcontrib><creatorcontrib>Schins, Roel P.F.</creatorcontrib><creatorcontrib>for the GINIplus and LISAplus study groups</creatorcontrib><creatorcontrib>GINIplus and LISAplus study groups</creatorcontrib><title>Air pollution and cytokine responsiveness in asthmatic and non-asthmatic children</title><title>Environmental research</title><addtitle>Environ Res</addtitle><description>Epidemiological studies indicate that asthmatic children are more susceptible to traffic-related air pollution exposure than non-asthmatic children. Local and systemic inflammation in combination with oxidative stress have been suggested as a possible susceptibility factor.
We investigated effect modification by asthma status for the association between air pollution exposure and systemic effects using whole blood cytokine responsiveness as an inflammatory marker.
The study was nested within the two German birth cohort studies GINIplus and LISAplus and initially designed as a random sub-sample enriched with asthmatic children. Using data from 27 asthmatic and 59 non-asthmatic six-year-old children we measured the production of Interleukin-6 (IL)-6, IL-8, IL-10, monocyte chemotactic protein-1 (MCP-1), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in whole blood after ex-vivo stimulation with urban particulate matter (EHC-93). Air pollution exposure (nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter with an aerodynamic diameter <10μm (PM10), particulate matter with an aerodynamic diameter <2.5μm (PM2.5mass), coarse particulate matter (PMcoarse) and PM2.5absorbance (PM2.5abs)) was modelled for children´s home addresses applying land-use regression. To assess effect modification by asthma status linear regression models with multiplicative interaction terms were used.
In asthmatics exposure to NO2 was associated with higher production of pro-inflammatory cytokines: adjusted means ratio (MR) 2.22 (95% confidence interval 1.22–4.04) for IL-6 per 2.68µg/m³ NO2. The interaction term between asthma status and NO2 exposure was significant. Results for NOx, PM10, PM2.5mass and PM2.5abs were in the same direction. No association between air pollution and cytokine responsiveness was found in the group of non-asthmatic children and in the overall group.
Traffic-related air pollution exposure is associated with higher pro-inflammatory cytokine responsiveness in whole blood of asthmatic children.
•We investigated the association between TRAP and systemic inflammation in asthmatic and non-asthmatic children.•Whole blood cytokine responsiveness was used as inflammatory marker.•TRAP is associated with higher pro-inflammatory cytokine responsiveness in asthmatic children.•No association was found in non-asthmatics.</description><subject>Air Pollutants - blood</subject><subject>Air pollution</subject><subject>Asthma</subject><subject>Asthma - chemically induced</subject><subject>Asthma - epidemiology</subject><subject>Blood</subject><subject>Child</subject><subject>Children</subject><subject>Cohort Studies</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Environmental Exposure</subject><subject>Environmental Monitoring</subject><subject>Exposure</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Germany - epidemiology</subject><subject>Humans</subject><subject>Inflammatory markers</subject><subject>Male</subject><subject>Models, Theoretical</subject><subject>Nitrogen dioxide</subject><subject>Nitrogen Oxides - blood</subject><subject>Particle Size</subject><subject>Particulate Matter - blood</subject><subject>Regression</subject><subject>Vehicle Emissions - analysis</subject><subject>Whole blood assay</subject><issn>0013-9351</issn><issn>1096-0953</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNqNkU1LAzEQhoMoWj_-gcgeveyaSXY3m4sg4hcIIug5bJNZmrpNarIt9N-b2qo39RQyeeYdMg8hp0ALoFBfTAt0y4CxYBSqgrKC8nKHjIDKOqey4rtkRCnwXPIKDshhjNN0hYrTfXLAKlFLYGJEnq9syOa-7xeD9S5rncn0avBv1mGWwufeRbtEhzFmNj3HYTJrB6s_Qedd_lPRE9ubgO6Y7HVtH_Fkex6R19ubl-v7_PHp7uH66jHXJWuGvK5ayYQAA4AtlZLzElMBOab_ILB6LLTgnDedQWZgXJpOSCoMjivAsmP8iJxvcufBvy8wDmpmo8a-bx36RVQgBGWSVU3zD5SzhtWyhL_RupZN2qhYp5YbVAcfY8BOzYOdtWGlgKq1IjVVG0VqrUhRppKi1Ha2nbAYz9B8N305ScDlBsC0vaXFoKK26DQaG1APynj7-4QPEW-jnw</recordid><startdate>201504</startdate><enddate>201504</enddate><creator>Klümper, Claudia</creator><creator>Krämer, Ursula</creator><creator>Lehmann, Irina</creator><creator>von Berg, Andrea</creator><creator>Berdel, Dietrich</creator><creator>Herberth, Gunda</creator><creator>Beckmann, Christina</creator><creator>Link, Elke</creator><creator>Heinrich, Joachim</creator><creator>Hoffmann, Barbara</creator><creator>Schins, Roel P.F.</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7ST</scope><scope>7T5</scope><scope>7TV</scope><scope>C1K</scope><scope>H94</scope><scope>SOI</scope><scope>8FD</scope><scope>FR3</scope><scope>KR7</scope></search><sort><creationdate>201504</creationdate><title>Air pollution and cytokine responsiveness in asthmatic and non-asthmatic children</title><author>Klümper, Claudia ; 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Local and systemic inflammation in combination with oxidative stress have been suggested as a possible susceptibility factor.
We investigated effect modification by asthma status for the association between air pollution exposure and systemic effects using whole blood cytokine responsiveness as an inflammatory marker.
The study was nested within the two German birth cohort studies GINIplus and LISAplus and initially designed as a random sub-sample enriched with asthmatic children. Using data from 27 asthmatic and 59 non-asthmatic six-year-old children we measured the production of Interleukin-6 (IL)-6, IL-8, IL-10, monocyte chemotactic protein-1 (MCP-1), tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in whole blood after ex-vivo stimulation with urban particulate matter (EHC-93). Air pollution exposure (nitrogen dioxide (NO2), nitrogen oxides (NOx), particulate matter with an aerodynamic diameter <10μm (PM10), particulate matter with an aerodynamic diameter <2.5μm (PM2.5mass), coarse particulate matter (PMcoarse) and PM2.5absorbance (PM2.5abs)) was modelled for children´s home addresses applying land-use regression. To assess effect modification by asthma status linear regression models with multiplicative interaction terms were used.
In asthmatics exposure to NO2 was associated with higher production of pro-inflammatory cytokines: adjusted means ratio (MR) 2.22 (95% confidence interval 1.22–4.04) for IL-6 per 2.68µg/m³ NO2. The interaction term between asthma status and NO2 exposure was significant. Results for NOx, PM10, PM2.5mass and PM2.5abs were in the same direction. No association between air pollution and cytokine responsiveness was found in the group of non-asthmatic children and in the overall group.
Traffic-related air pollution exposure is associated with higher pro-inflammatory cytokine responsiveness in whole blood of asthmatic children.
•We investigated the association between TRAP and systemic inflammation in asthmatic and non-asthmatic children.•Whole blood cytokine responsiveness was used as inflammatory marker.•TRAP is associated with higher pro-inflammatory cytokine responsiveness in asthmatic children.•No association was found in non-asthmatics.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>25769127</pmid><doi>10.1016/j.envres.2015.02.034</doi><tpages>10</tpages></addata></record> |
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| ispartof | Environmental research, 2015-04, Vol.138, p.381-390 |
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| subjects | Air Pollutants - blood Air pollution Asthma Asthma - chemically induced Asthma - epidemiology Blood Child Children Cohort Studies Cytokines Cytokines - metabolism Environmental Exposure Environmental Monitoring Exposure Female Flow Cytometry Germany - epidemiology Humans Inflammatory markers Male Models, Theoretical Nitrogen dioxide Nitrogen Oxides - blood Particle Size Particulate Matter - blood Regression Vehicle Emissions - analysis Whole blood assay |
| title | Air pollution and cytokine responsiveness in asthmatic and non-asthmatic children |
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